The study was conducted as a cross-sectional analysis from December 2022 to November 2023 to examine the prevalence of cataracts among diabetic patients and evaluate the association with smoking and hypertension. This design allowed for the assessment of exposure and outcome variables simultaneously at a single point in time.

Research activities were carried out in a single healthcare facility with a specialized diabetes and ophthalmology unit, facilitating the recruitment of diabetic patients and the evaluation of cataract status alongside smoking and hypertension variables.

The total study population comprised 60 diabetic patients. Among these, 32 patients were diagnosed with cataracts (case group), and 28 patients did not have cataracts (control group). Eligibility criteria for participants were refined to include only active smokers with a history of smoking for 5 years or more and patients with hypertension diagnosed based on the criteria of the American Heart Association, with a history of hypertension for at least 5 years.

All participants were aged 18 years and older, with a confirmed diagnosis of Type 1 or Type 2 diabetes. Patients with cataracts due to other systemic diseases, medications, trauma, or congenital factors were excluded from the study to isolate the impact of diabetes, smoking, and hypertension on cataract development.

The presence of cataracts was the primary outcome, determined through ophthalmological examinations by qualified ophthalmologists using slit-lamp biomicroscopy. Information on smoking status and hypertension was collected through patient interviews and medical record reviews.

Data on demographics, smoking history, hypertension status, diabetes management, and ophthalmologic findings were collected through structured interviews and review of medical records. This approach ensured comprehensive data collection on all relevant variables. Additionally, the cataract was evaluated using the (Carl Zeiss Meditec AG) 220 slit lamp manufactured in Jena, Germany with a serial number of (9707200663).

Descriptive statistics summarized the demographic and clinical characteristics of the participants. The prevalence of cataracts in the study population was calculated, and the association between cataract development and risk factors such as smoking and hypertension was analyzed using logistic regression models. Adjustments were made for potential confounders including age, duration of diabetes, and glycemic control. Odds ratios (ORs) and 95% confidence intervals (CIs) were reported to quantify the strength of associations.

The findings indicate that smoking does not significantly affect the development of cataracts among diabetic patients. With a p-value of 0.885 and an odds ratio of 1.187, the results suggest a negligible impact of smoking on cataract incidence. This contradicts some previous studies which have suggested a potential link between oxidative stress induced by smoking and cataract formation. ¹⁶ One of the mechanisms of lens damage and cataract formation is disruption of the protective function of alpha crystalline, a vital protein in the lens that acts as a chaperone to prevent the aggregation of denatured proteins, which can lead to light scattering and opacity in the lens. ¹⁷ P-parabenzoquinone which is a compound found in cigarette smoke, disrupts the structure of alpha-crystalline, contributing to cataract formation. ¹⁸ Moreover, smoking directly exposes the lens epithelial cells to harmful toxins and indirectly decreases levels of antioxidant molecules, like ascorbic acid and nicotinamide. Heavy metals present in cigarettes, such as lead and cadmium, further exacerbate oxidative stress by depleting crucial antioxidant defenses like glutathione. ^{18 , 19}

The impact of smoking on cataract formation has been widely documented ^{20 , 21} ; however, the effect size can vary significantly depending on individual smoking behaviors. ²² The inconsistency in the smoking impact might also be attributed to variations in the duration, intensity, and cessation of smoking habits among the subjects in this study. This variation could dilute the observable impact of smoking on cataract development in a relatively small cohort. Furthermore, as cessation timing varies among individuals, the cumulative exposure to the harmful components of tobacco smoke necessary to influence cataract pathogenesis may not have been reached uniformly across this study sample. This aligns with the existing literature that provides evidence of a dose-response effect of smoking on ocular morbidity. ²³ This is due to several factors. Higher smoking intensity can exacerbate oxidative stress, leading to increased damage to proteins in the lens. This damage disrupts various cellular processes crucial for repair and recovery. Over time, this cumulative damage not only affects the lens but also extends to other ocular tissues. ^{23 , 24}

Although the prevalence of hypertension was higher in the cataract group, the statistical analysis (p-value of 0.146) failed to show a significant correlation. The odds ratio of 2.277 suggests a potential trend or risk association, yet the confidence intervals and the high p-value underscore a lack of statistical certainty. Hypertension has been previously identified as a risk factor for cataracts development. ²⁵ It triggers an inflammatory response in the eye, leading to elevated levels of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6), and C-reactive protein (CRP). This chronic inflammatory state contributes to oxidative stress and cellular damage within the lens, accelerating cataract formation. ^{26 , 27} Hypertension also directly impact the structure of lens proteins, as proposed by Lee et al., ²⁸ potentially exacerbating protein aggregation and lens opacity. Additionally, experimental animal studies have implicated the renin-angiotensin system, a key regulator of blood pressure, in the pathogenesis of cataracts. ²⁹ Ornek et al. ³⁰ demonstrated that elevated nitrite levels in cataractous lenses of hypertensive patients is crucial in cataracts formation. Interestingly, several studies have suggested an association between hypertension (HTN) and cataract formation, partly attributed to the use of anti-hypertensive medications. Cumming et al. ³⁰ highlighted a significant link between cataract risk and potassium-sparing diuretics, which aligns with biological plausibility. These anti-HTN drugs have the potential to disturb the electrolyte balance across lens fibers, thereby contributing to cataract development. The lack of significant findings in the present study might suggest that while hypertension could contribute to cataracto genesis, its effect might be less direct and perhaps mediated by other diabetic complications or vascular factors that were not controlled for in this analysis.

The study has some limitations that warrant consideration. Firstly, the sample size of 60 participants may limit the generalizability of the findings and the statistical power to detect small effect sizes. Secondly, the cross-sectional design of the study precludes conclusions about causality between smoking, hypertension, and cataract development. Additionally, the reliance on self-reported data for smoking and hypertension status could introduce recall bias and misclassification, potentially obscuring true associations.